作者: Bernard C. Wexler
DOI: 10.1016/0002-8703(70)90395-9
关键词: Heart failure 、 Prostration 、 Endocrinology 、 Edema 、 Serum creatine phosphokinase 、 Shock (circulatory) 、 Cellular infiltration 、 Internal medicine 、 Arteriosclerosis 、 Myocardial infarction 、 Medicine 、 Cardiology and Cardiovascular Medicine
摘要: Abstract Male and female rats with without arteriosclerosis were given two subcutaneous injections of isoproterenol spaced 24 hours apart. The animals promptly developed signs shock prostration myocardial infarction. Sequential sacrifice the at hourly intervals after each demonstrated that there was a prompt marked increase in serum creatine phosphokinase (CPK) activity commensurate destruction tissue. Serum CPK levels elevated long before microscopic examination myocardium could demonstrate any evidence overt muscle damage, indicating enzyme is sensitive index not only necrosis but sarcolemmal membrane permeability as well. changes much more dramatic these experiments than previous experience where other enzymes used to detect infarction, e.g., transaminases (SGOT SGPT) lactic dehydrogenase. Female showed severe untoward connection infarction males. Yet subjects survived greater numbers rapid effective repair heart male subjects. This dichotomous response between sexes also reflected pattern response. Animals having pre-existing prior being subjected isoproterenol-induced show excursion their normal arteries. However, presence per se no way contributed levels. Therefore, it suggested extra elevation arteriosclerotic reflection intrinsic damage such despite fact they manifest less failure Heart weight greatly increased during acute episode oscillations on an hour-by-hour basis. Histologic indicates this cardiac size due cellular infiltration, edema possible electrolyte abnormalities, permeability.